Factors contributing to altered left ventricular diastolic properties during angina pectoris.

Mann, Tift; Goldberg, S. A.; Mudge, Gilbert H.; Grossman, William

doi:10.1161/01.cir.59.1.14

Cited by 235 publications

(79 citation statements)

References 50 publications

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“…Coronary artery disease (CAD) has been implicated in the pathogenesis of HFNEF; ischaemia prolongs τ, which is reversed after reduction of ischaemic burden by coronary artery bypass grafting 26 , 27 , 28 . Mann, et al 26 showed that in CAD, ischaemia provocation by rapid atrial pacing resulted in an upward shift of the diastolic pressure‐volume curve.…”

Section: Likely Mechanisms For Diastolic Dysfunctionmentioning

confidence: 99%

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Echocardiographic evaluation of diastolic heart failure

Thomas

2010

Australas J Ultrason Med

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Section: Likely Mechanisms For Diastolic Dysfunctionmentioning

confidence: 99%

“…Mann, et al 26 showed that in CAD, ischaemia provocation by rapid atrial pacing resulted in an upward shift of the diastolic pressure‐volume curve.…”

Section: Likely Mechanisms For Diastolic Dysfunctionmentioning

confidence: 99%

Echocardiographic evaluation of diastolic heart failure

Thomas

2010

Australas J Ultrason Med

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“…10,42,43 The pressure-volume changes during ischemia also indicate a change in distensibility of the ventricle. 44 All these findings point to a mechanical influence, namely stretch, in the nU genesis. 9,13,16,27 The transitory inducibility of the nU by acute supply ischemia during PTCA offers an experimental model in humans that may help explain its pathogenesis.…”

Section: Pathogenesis Of the Negative U Wavementioning

confidence: 96%

“…Among the former are the completeness of ventricular relaxation and the passive fibroelastic properties of the ventricle; among the latter are coronary arterial pressure, flow, and right ventricular loading. 44 During acute supply ischemia, the intrinsic components are certainly altered, but the extrinsic ones particularly so. In fact, normally 15% of the ventricular wall is composed of coronary blood, 47 which contributes to its mass and tone.…”

Section: Pathogenesis Of the Negative U Wavementioning

confidence: 99%

The negative U wave: A pathogenetic enigma but a useful, often overlooked bedside diagnostic and prognostic clue in ischemic heart disease

Correale¹,

Battista²,

Ricciardiello³

et al. 2004

Clinical Cardiology

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Summary:The pathogenesis of U-wave inversion and its clinical value are still not clear, although the U wave was described by Einthoven together with the other electrocardiographic (ECG) waves. Not considered a useful diagnostic clue, it is not usually mentioned in ECG reports. In recent years, stimulated by the long QT syndromes and by the discovery of U-wave changes in some pathologic, mostly cardiac states, this neglected wave has attracted new interest. This review focuses on the negativity of the U wave in ischemic heart disease. The discovery of M cells and their electrophysiology has established the cellular basis for repolarization and has contributed to our knowledge of U-wave genesis. Hemodynamic changes during diastole in acute ischemia also furnish interesting elements for the interpretation of U-wave changes, and some experimental and clinical studies, besides designating stretch as a cause of U-wave changes, have also proved their value for more accurate bedside diagnosis and prognosis. They may indicate the extent of myocardial ischemia, the presence of collateral circulation, and the possible territory and vessel involved. When U-wave changes are the first and only sign of ischemia, they may contribute to a decision regarding the hospital admission of a patient without typical ischemic symptoms. Furthermore, U-wave changes during exercise tests increase their sensitivity.

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“…'`These observations suggest that the increase in left ventricular diastolic pressure during angina may be related to impaired inactivation of the myosin-actin interaction in ischemic myocardium.2' 13 On the other hand, regional dyssynchrony of ischemic and nonischemic segments is an alternate mechanism that has been proposed. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] In contrast to patients with coronary artery disease, patients with aortic stenosis who develop angina during exercise or pacing tachycardia are likely to do so in response to diffuse global left ventricular subendocardial ischemia rather than segmental ischemia. Coronary vascular reserve appears to be impaired in many patients with pressure-overload hypertrophy due to aortic stenosis who do not have coronary artery dis- 17 19 ease and in dogs with chronic aortic stenosis.…”

mentioning

confidence: 99%

Altered left ventricular diastolic properties during pacing-induced angina in patients with aortic stenosis.

Fifer¹,

Bourdillon²,

Lorell³

1986

Circulation

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An increase in left ventricular diastolic pressure has been repeatedly observed during angina in patients with coronary artery stenoses and regional demand ischemia, but the role of relaxation abnormalities versus left ventricular segmental dyssynchrony is controversial. In contrast, patients with angina due to aortic stenosis are likely to have diffuse rather than segmental ischemia and thus may provide an alternative model for examining the diastolic physiology of angina in man. Accordingly, we examined the hemodynamic manifestations of angina in eight patients with aortic stenosis without significant coronary artery disease. Angina was induced by pacing tachycardia, and hemodynamic and echocardiographic variables were measured in the control period and during angina in the beats immediately after cessation of pacing. Heart rate (control vs angina, 69 + 12 vs 70 + 11 beats/min, p = NS) and left ventricular peak systolic pressure (207 39 vs 222 22 mm Hg, p = NS) were similar in the control and postpacing angina periods. Left ventricular end-diastolic pressure, on the other hand, was significantly higher during postpacing angina (15 ± 7 vs 28 8 mm Hg, p < .01). The time constant of left ventricular pressure decline during isovolumetric relaxation (TL), calculated as the slope of a linear fit of the natural log of pressure vs time, increased from 44 + 5 to 51 + 7 msec (p < .05); the time constant TD, derived from the slope of a linear fit of dP/dt vs pressure, also increased slightly, although the change was not statistically significant (69 + 5 vs 75 + 5 msec, p = .06). High-quality two-dimensional targeted M mode echocardiograms in the control and postpacing periods were available in four patients; left ventricular end-diastolic and end-systolic dimensions and percent fractional shortening were unchanged. The left ventricular diastolic pressure-volume relationship and pressure-wall thickness relationship were shifted upward during angina in these patients. We conclude that angina in patients with aortic stenosis is accompanied by a substantial and reversible increase in left ventricular end-diastolic pressure; this increase appears to be due in part to an impairment of diastolic distensibility of the left ventricle and left ventricular relaxation. These findings, which are similar to those observed during pacing-induced angina in patients with coronary stenoses, suggest that the increase in left ventricular end-diastolic pressure that occurs during angina is a manifestation of demand ischemia per se, and does not depend on the presence of dyssynergistic contraction of ischemic and nonischemic regions. Circulation 74, No. 4, 675-683, 1986. ANGINA is a common symptom in patients with aortic stenosis, and is frequently the presenting complaint.'In patients with coronary artery disease, angina provoked by exercise or pacing tachycardia is often ac-

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Factors contributing to altered left ventricular diastolic properties during angina pectoris.

Cited by 235 publications

References 50 publications

Echocardiographic evaluation of diastolic heart failure

Echocardiographic evaluation of diastolic heart failure

The negative U wave: A pathogenetic enigma but a useful, often overlooked bedside diagnostic and prognostic clue in ischemic heart disease

Altered left ventricular diastolic properties during pacing-induced angina in patients with aortic stenosis.

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